Blood Pressure and Flow Overview emphasis on SYSTEMIC CIRCUIT Source of pressure Modifies pressure Perfuses tissues with blood, Maintains flow to cappilaries Returns blood to heart

Fig Capillary bed

BLOOD FLOW Blood flows from high pressure areas to low pressure areas Blood flows through vascular system because of these pressure differences Arteries  arterioles  capillaries  venules  veins High pressure, no exchange Low pressure, exchange occurs low pressure, “no exchange”

Fig As arteries and arterial branch and vessels become more numerous, pressure decreases and stays low until pumped through heart again.

Total Area ->pressure->velocity Venous lower then arterial relate to relative fractions in arterial v. venous components

Fig Distribution of blood within vessels Average Blood Volume = 5-6L Systemic Circuit = ~ 77% of all blood volume Venous system represents a reservoir of blood that can be shunted to the arterial portion of the system

About 5-6L of blood in average person Systemic circuit = 77% of all blood in vessel

Systole Diastole MAP Elastic Rebound

Fig Vessel-Pressure Patterns Pulsation and overall pressure decrease with distance Pulsation due to heart gone by capillaries Capillaries and veins are low pressure vessels key for regulating BP

Arterial Flow Systemic arterial pressure ranges from mmHg This pressure ensures blood flow through capillaries where exchange happens Vasoconstriction/Dilation 1. Regulates blood pressure Constriction/dilation of arterioles is most important –Constriction increases Resistance  increases BP –Dilation decreases resistance  decreases PB 2. Shunts blood (re-distributes it) to parrallel “circuits”/other places

Figure 23.5 artery arteriole Capillary bed venule veins

Capillary flow Low pressure –35mmHg-18mmHg Capillary beds –interconnected networks of capillaries Local flow/vasomotion –flow through capillaries is not constant, but is regulated by precapillary sphincters (and terminal arterioles) –Only 25% of capillaries experiences flow at any moment (at rest) Vessels are permeable –Capillary exchange

Capillary Exchange Diffusion/osmosis (due to concentration gradients) –Between gaps in cells (ions and small organic molecules) –Through transport proteins (ions) –Through membrane lipids (lipid soluble substances) Filtration due to: capillary hydrostatic pressure (i.e., blood pressure in capillaries) 35-18mmHg –Primarily at arterial end of capillary drives net filtration out of vessels (~ 35 mmHg) Osmotic pressure (colloid osmotic pressure/oncotic pressure) –drives reabsorption of most fluid lost by filtration –Minimized by reabsorption due to colloid osmotic pressure –Primarily at venous end of capillary (~ 18 mmHg) Active Transport –Ion pumps –Vessicular transport: endocytosis brings materials into one side of endothelium and released to opposite site by exocytosis

Fig If capillary hydrostatic pressure rises  increased filtration and accumulation of fluid in interstitial space=edema If blood volume declines due to bleeding, capillary hydrostatic pressure/filtration declines  increased reabsorption (partially compensating volume loss) During dehydration colloid osmotic pressure increases  increased reabsorption (partially compensating volume loss)

Fig Net loss of fluid from capillaries results in fluid flow: –Plasma  –interstitial space/fluid  –lymph  –plasma “ flushes interstitial fluid enhancing immune system function Keeps interstitial fluid and plasma in “communication” Increases distribution of materials especially insoluble lipids that have difficulty crossing capillary walls

Fig Fluid lost from plasma enters lymph and is eventually returned to plasma –No loss of plasma volume –3.6L/day transported as lymph Lost from capillaries

Fig

Venous Flow Low pressure 18mmHg – 2mmHg Non-pulsile Venous reservoir Flows due to –Small pressure gradient –Muscle pump (skeletal muscle contraction particularly the lower limbs) –Respiratory pump Contraction of diaphragm enhances venous return

Muscle pump: Constriction muscles compresses veins and pressurizes blood Valves ensure this blood moves towards heart Increased muscle use  increased venous return

Regulation of Arterial Flow Extrinsic regulation –SD-ANS –Hormones Intrinsic (autoregulation) Regulation of local flow The state of vasoconstriction/dilation and blood flow (and is due to the combined effects of both autoregulation and extrinsic regulation

Neuroendocrine regulation of BP and Blood Flow Autoregulation of local flow

Nervous System Regulation Vasoconstriction/Dilation Sympathetic Divison ANS (Vasomotor Centers of Medulla) –Adrenergic Fibers (neurons) –Most vessels (including skeletal muscle, see below) –NE to alpha 1 receptors  constriction –Sympathetic Tone—default state of partial contraction due to normal “background” SD activity –Increased SD  –Decreased SD  Cholinergic Fibers (neurons) –Primarily Skeletal muscle Note skeletal muscle vessels have sypathetic tone due to alpha andrenergic innervation –Ach to cholinergic receptors  Dilation –Skeletal muscle cells also have beta 2 adrenergic receptors that are stimulated by epinephrine released by adrenal medulla that promote dilation.

Sympathetic tone, vasoconstriction and vasodilation Rate of SD signaling

Autoregulation/Intrinsic Regulation of local blood flow local factors (including paracrine regulation)  changes in capillary bed flow –Due to constriction/dilation of precapillary sphincters and arterioles Factors decrease O2/increase CO2 increase lactic acid/decrease pH NO increase K+ increase histamine release increase temperature increased stretch of vascular smooth muscle prostoglandins & thromboxanes promote dilation / increase flow promote constriction / decreased flow released during tissue damage and during clotting Myogenic mechanisms

Fig Constriction: reduces flow to “down stream” structures Increases pressure and flow to “upstream” structures. Reduced flow Increased pressure and flow

Regulation of BP Blood Pressure Influenced by: CO –Heart function Vascular Resistance –more resistance = increased BP Diameter of vessels –dilation  reduces resistance/BP Length of vessels Viscosity of blood Blood volume –influenced by water balance (water uptake v. water loss) Changes in minutes Changes in hours-days

Page 470 Vasoconstriction Vasodilation Blood Volume Primary factors influencing BP

Blood Flow and Regulation of Systemic BP Blood must flow to tissues that need it –BP must be sufficient to deliver blood adequately Perfussion –lack of perfusion  Ischemia/ischemic  infarction Regulation of BP Intrinsic/Autoregulation of local flow Extrinsic Regulation –Nervous system—sympathetic ANS Medulla: vasomotor center –Endocrine System/Hormonal regulation Mostly long term regulation of blood volume Hypothalamus  pituitary  Kidneys

Fig SV and CO

Overview of cardiovascular regulation

Baroreceptor reflex Baroreceptors (pressure) in carotid bodies and aorta –Glossopharyngeal nerve (carotid bodies) –Vagus nerve (aorta) –Detect increases and decreases in pressure Send sensory impulses to medulla –Cardiac center sends output to heart—re: CO SD (cardioaccelaratory) and PD (cardioinhibitory) –Vasomotor center send output to vessels—re: constriction/dilation SD BP maintained within normal range

Fig

Orthostatic/postural hypotension and barocrecptor reflex

Neural responses to changes in BP SD PD SD PD SD ↑BP ↓BP VIS: very important slide

Endocrine/Hormonal Regulation of BP Mostly through regulation of blood volume –But also vasoconstriction/dilation effects Hormones Antidiuretic Hormone (ADH, vasopressin) Angiotensin II Aldosterone Natriuretic Peptide

Fig ADH Decreasing blood/plasma volume  increased solute concentration (osmolality) ADH release increases Increased fluid retention (less urine output) Increased water intake Blood volume stabilized/increased

Fig Angiotensin II decreased Renal blood pressure Angiotensin II release Vasoconstriction –Short term BP increase/stabilizer Aldosterone released –Increased water retention (less urine output) –Increased/stabilized blood volume Increased/stabilized BP *ACE inhibitors for hypertension

Response to ↓ blood vol./pressure Combined influence of –ANS—SD –ADH –Angiotensin II –Aldosterone Censored

Fig Natriuretic Peptides and Increased BP High BP  Stretches atria Natriuretic peptide release Inhibits ADH release Increases water loss/urine output Blood volume decreases BP decreases

Response to ↑ blood vol/pressure.

Changes in Systemic Blood Distribution With Exercise

Physiological (circulatory) Shock Inadequate perfusion (blood flow/BP) 3 fundamental causes Heart: insufficient CO  BP inadequate –Infarction, severe arrhythmias or valve damage Vessels: widespread vasodilation  BP inadequate –Brain damage, endotoxins, or histamine (allergic rxn) Blood Volume: too low  BP inadequate –Bleeding, burns, dehydration

Table 14.4

Table 14.5

Fig